SEATTLE — Diet appears to have some influence on the levels of proteins and peptides related to development of Alzheimer’s disease, according to a study led by researchers from the VA’s Puget Sound Healthcare System.1

The report, published online by JAMA Neurology, noted that Alzheimer’s is caused in part by the accumulation of β-amyloid (Αβ) peptides in the brain, which can be bound to lipids or lipid carrier proteins, such as apolipoprotein E (ApoE), or be free in solution (lipid-depleted [LD] Αβ).

Angela J. Hanson, MD, who also is associated with the University of Washington, Seattle, and colleagues studied 20 older adults with normal cognition — averaging 69-years-old — and 27 older adults with amnestic mild cognitive impairment — averaging 67 years old. Study subjects were randomized either to a diet high in saturated fat content (45%t energy from fat, greater than 25%t saturated fat) with a high glycemic index or to a diet low in saturated fat content (25% of energy from fat, less than 7% saturated fat) with a low glycemic index. Lipid depleted (LD) Αβ42 and Αβ40 and ApoE in cerebrospinal fluid were used as the main outcome measurements.

Baseline levels of LD Αβ were found to be greater for adults with mild cognitive impairment compared with adults of normal cognition, according to the authors who also noted that these findings were more apparent in adults with mild cognitive impairment and the Ɛ4 allele (a risk factor for AD), who had higher LD apolipoprotein E levels, regardless of cognitive diagnosis. The diet low in saturated fat tended to decrease LD Αβ levels, while the diet high in saturated fat increased these fractions.

“Overall, these results suggest that the lipidation states of apolipoproteins and amyloid peptides might play a role in AD pathological processes and are influenced by APOE genotype and diet,” according to the authors, who cautioned that the small pilot study needs to be replicated in a larger sample.

“Hanson et. al argue that the changes observed after their two dietary interventions may underlie some of the epidemiologic findings regarding diabetes and other cardiovascular risk factors and risk for AD. The specifics of their model may not capture the real underlying biological effect of these diets, and it is unclear whether the observed changes in the intermediate outcomes would lead to beneficial changes in oligomers or plaque burden, much less to decreased brain atrophy or improved cognition,” she continued.

Blacker suggested that the “important lesson from the study is that dietary intervention can change brain amyloid chemistry in largely consistent and apparently meaningful ways — in a short period of time. Does this change clinical practice for those advising patients who want to avoid dementia? Probably not, but it adds another small piece to the growing evidence that taking good care of your heart is probably good for your brain, too.”